The fastigial nucleus in the cerebellum has been shown to elicit powerful cardiovascular changes during electrical stimulation. Hypertension, tachycardia, increased myocardial contractility and coronary artery flow are among the effects observed in three species to date. However, the normal operative function of this nucleus and its potential involvement in idiopathic hypertension is unknown at the present time. The chronically instrumented dog model will be used to examine both short and long-term cardiovascular alterations during acute stimulation and low-grade, chronic stimulation. The physiological role of the nucleus in cardiovascular responses to submaximal exercise will be studied in the conscious instrumented dog performing treadmill exercise before and after unilateral and bilateral lesioning in discrete portions of the nucleus. Indwelling multipolar brain electrodes and cardiac instrumentation such as pressure cells. Doppler blood flow transducers and sampling catheters in the absence of anesthesia allow for a physiological approach to the study of pathways involved in cardiovascular control. Recent anatomical studies have implicated fastigial nucleus with receiving information concerning orthostatic tolerance from vestibular nuclei and information concerning muscle activity from flexor reflex afferents. The nucleus sends efferents to medullary reticular formation nuclei affecting descending sympathetic cardiovascular regulation (lateral reticular nucleus, paramedian reticular nuclus) and nuclei proven to be involved with baroreceptor feedback mechanisms (parasolitary nucleus of tractus solitarius). Consequently, the possible modulation of descending sympathetic pathways or resetting of incoming baroreceptor information make the fastigial nucleus a model candidate in neurogenic hypertension. Histological studies, including degeneration tracking techniques will be used to verify the cerebello-medullary pathways involved.